Body response to trauma, wound healing and wound management

7/30/2019 Body response to trauma, wound healing and wound management

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Dr.Khalid Al.Zahrani

Assistant professor and consultant plastic surgeon

King Khalid University Hospital.


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Inflammatory response to injury to restore tissue function

Eradicate invading microorganisms

Local- limited duration, restores function Major

overwhelming inflammatory response

Potential multi-organ failure

Adversely impacts patient survival


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Endocraine.

Metabolic.

Immunologic.


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Activated by: Injured tissue:

Mediators: TNF alpha

Neural.

Intravascular volume depletion.

2 main types: Hypothalamic-pituitary control.

Autonomic nervous system.


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Pain, Fear, Anxiety Mediators from IT Nociceptors Baroreceptor

HypothalamicPituitary Axes

AutonomicAxes

ACTHCortisolAldesterone

TSHGHProlactinEndo-OpiodsADH

AD/NAAldesteroneInsulinGlucagon

Target Organ

Cell SurfaceReceptors

IntracellularReceptors


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Hormone classifications polypeptide (cytokine, insulin)

amino acid (epinephrine, serotonin, or histamine)

fatty acid (cortisol, leukotrienes)


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Synthesized anterior pituitary

Regulated by circadian signals

Pattern is dramatically altered in injured patients

Elevation is proportional to injury severity Released by: pain, anxiety, vasopressin,

angiotensin II, cholecystokinin, catecholamines, and pro-inflammatory cytokines

ACTH signals increase glucocorticoid production


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Cortisol elevated following injury, duration of elevation depends on severity of injury

Potentiates hyperglycemia

Hepatic gluconeogenesis Muscle and adipose tissue > induces insulin resistance

Skeletal m.> protein degradation, lactate release

Adipose -> reduces release of TG, FFA, glycerol


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GH: Protein synthesis.

Fat mobilization.

Hyperglycemia.

Immunostimulatory.


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During stress -> protein synth, fat mobilization, andskeletal cartilage growth

2 to release of insulin-like growth factor (IGF1)

Injury reduces IGF1 levels IGF1 inhibited by pro-inflammatory cytokines

TNF-, IL-1, IL-6

GH admin to pediatric burn patients shows

improvement in their clinical course


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Catecholamines.

Aldosterone.

Renin-angiotensin.

Insuline. Glucagon.


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Severe injury activates the adrenergic system Norepi and Epi immed. increase 3-4 fold and remain

elevated 24-48hrs after injury

Epinephrine hepatic glycogenolysis, gluconeogenesis, lipolysis, and

ketogenesis Decreases insulin and glucagon secretion Peripheral- lipolysis, insulin resistance in skeletal m.

= stress induced hyperglycemia


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Synthesized, stored, released from the adrenal zonaglomerulosa

Maintains intravascular volume

Conserves sodium Eliminates potassium and hydrogen ions

Acts on the early distal convoluted tubules

Deficiency- hypotension, hyperkalemia

Excess- edema, HTN, hypokalemia, metab alkalosis


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Stress inhibited release + peripheral insulin resistance= hyperglycemia

Injury has 2 phases of insulin release Within hours- release is suppressed Later- normal/xs insulin production with peripheral

insulin resistance

Activated lymphocytes have insulin receptors ->enhanced Tcell proliferation and cytotoxicity

Tight control of glucose levels esp. in diabeticssignificantly reduces mortality after injury


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EbbPhase Flow Phase

Injury

Catabolism

Anabolism

Death

Minutes

Hours DaysWeeks

Energy

Temperature

O2 Consumption


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Energy balance: Increased energy expenditure and oxygen consumption.

Lipid metabolism: Lipolysis.

Carbohydrates: Hyperglycemia.

Protein and AA:

Increased break down.


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Wound: a disruption of normal anatomic relations as aresult of injury intentional or unintentional.Regardless of causation or tissue type, wound healingpresents with identical biochemical and physiologic

processes, though wound healing may vary in timingand intensity.


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Substrate or reactive phase, immediatetypicallydays 1-10

Response to limit and prevent further injury,inflammation, hemostasis, sealing surface,removing necrotic tissue and debris,migration of cells into wound by chemotaxis,cytokines, and growth factors

Initial intense localvasoconstriction of arteriolesand capillaries followed by vasodilation and

vascular permeability


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Tissue injury & blood vessel damage

exposure ofsubendothelial collagento platelets andvWF activatesthe coagulation pathway

Plugging: Platelet and fibrinProvisional matrix:platelets, fibrin, and fibronectinPlatelet aggregation:Thromboxane (vasoconstrict),

thrombin, platelet factor 4


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Alpha granules contain:

-platelet factor 4: aggregation-Beta-thrombomodulin: binds

thrombin

-PDGF: chemoattractant-TGF-beta: key component tissue repair

Dense granules containvasoactive substances:adenosine, serotonin, and calcium

Other factors released: TXA, Platelet activatefactor, Transform. growth factor alpha, Fibroblast

growth factor, Beta lysin (antimicrobial), PGE2

and PGI2 (vasodilate) and PGF2 (vasoconstrict).


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Chemotaxins attract after extravasation

Migrate through the ECM by transientinteraction with integrins

PMNs scavenge, present antigens,

provide cytotoxicity-free radicals (H2O2)Migration PMNs stops with woundcontamination control usually a few days

Persistant contaminant: continuous influxPMNs and tissue destruction, necrosis,abscess, & systemic infection

PMNs are not essential to wound healing


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Monocytes migrate &

activate: Macrophages

Appear when PMNsdisappear 24-48 hr

Do the same activities as PMNsPlus orchestrate release of enzymes(collagenase, elastase), PGEs,

cytokines (IL-1, TNF alpha,IFN ), growth factors (TGF& PDGF), and fibronectin

(scaffold/anchor for fibroblasts)Activate Fibroblasts, endothelial andepithelial cells to form Gran. Tissue


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Fibroblasts

differentiatefrom restingmesenchymalcells in connective

tissue

3-5 days migrate fromwoundedge

Fibroplasia: Fibroblasts

proliferate replace

fibronectin-fibrinwith

collagen contribute ECM


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I(80%

skin)

Most Common: skin,

bone, tendon.

Primary type in

wound healing.

II Cartilage

III(20 %skin)

Increased Ratio inhealing wound, also

blood vessels and skin

IV Basement Membrane

V Widespread,

particularly in the

cornea

Type III predominant collagensynthesis days 1-2Type I days3-4Type III replaced by Type I in3

weeks


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6 Week = 60% original,80% final strength

8 Week-1year 80%

original (Max)Net Collagen = 6 weeksamount stays thesame but cont.

crosslink increasestrength = maturation


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Remodeling of wound3 week-1+year

Type I replaces Type III Collagen: net amount doesntchange after 6 weeks, organization & crosslinking

Decreased vascularity, less fibroblasts & hyaluronicacid

Peripheral nerves regenerate @ 1mm/day

Accelerated Wound Healing: reopening results inquicker healing 2nd time around


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Contraction: centripetalmovement of the wholethickness of surrounding skin

reducing scarMyofibroblasts: specialFibroblasts express smoothmuscle and bundles of actin

connected through cellularfibronexus to ECM fibronectin,communicate viagap junctionstopull edges of the wound

Contracture: the physicalconstriction or limitation offunction as the result ofContraction (scars across

joints, mouth, eyelid)

Burn/Keloid causingcontracture


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Excess Deposition ofCollagen Causes Scar

Growth Beyond theBorder of theOriginal wound

Tx: XRT, steroids, silicone sheeting, pressure,excise. often Refractory toTx & not preventable

Autosomal Dominant,Darker Pigment, Often

above clavicle but notalwa s


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Excess collagen deposit causingraised scar remains within theoriginal wound confines

Darker pigmented skin & flexorsurfaces of upper torso

Often occurs in burns or woundsthat take a long time to heal,sometimes preventable

Can regress spontaneously

Tx: steroids, silicone, pressuregarments


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Diabetes: impedes the early phase

response

Malnurishment:Albumin


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Osteogenesis Imperfecta: Type I Collagen defectEhler-Danlos syndrome: Collagen disorder, 10 types

Marfan Syndrome: fibrillin defect (collagen)

Epidermolysis Bullosa: Excess fibroblasts Tx:phenytoinScurvy:Vit C req. for proline hydroxylation


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Thank you

Body response to trauma, wound healing and wound management

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